Abstract
Tumor necrosis factor-α (TNF-α) had been identified as a key pro-inflammatory cytokine in the pathophysiology of major depressive disorder (MDD) and the mechanism of antidepressant treatment. The primary aim of the present study was to examine the serum TNF-α levels in Chinese inpatients with MDD during the acute phase and to explore the changes in TNF-α levels after effective clinical treatment. Fifty-seven consecutive inpatients with MDD and 30 healthy controls were recruited. The serum TNF-α levels were detected using ELISA. Symptoms of depression were evaluated using the 24-item Hamilton Rating Scale for Depression (HAM-D-24). TNF-α levels and HAM-D-24 scores were assessed at baseline and after 2 and 12 weeks of follow-up. The serum TNF-α levels were higher in the MDD group than in the control group. After 2 and 12 weeks of antidepressant treatment, there were significant improvements in the patients' symptoms and significant decreases in the TNF-α levels. The baseline TNF-α levels significantly correlated with the decreased HAM-D-24 scores, particularly for the depressive symptoms of anxiety/somatization and weight loss. The present findings indicate that depression is accompanied by activation of TNF-α, which also has a predictive value for the antidepressant treatment response in patients with MDD.
Highlights
Major depressive disorder (MDD) has emerged as one of the most common psychiatric disorders [1]
The present study explored by setting up multiple follow-up points to examine the dynamic changes in the serum Tumor necrosis factor-α (TNF-α) levels in a fairly homogeneous group of major depressive disorder (MDD) patients treated with antidepressants in clinical settings
The primary aim of the current study was to examine the difference in the serum TNF-α levels in Chinese inpatients with MDD in the acute phase with healthy controls and, more importantly, to explore the changes in TNF-α levels and their predicting value for effective antidepressant treatment
Summary
Major depressive disorder (MDD) has emerged as one of the most common psychiatric disorders [1]. The inflammatory cytokine system is activated in several somatic diseases that share a number of common symptoms with MDD, such as tiredness. This implies that inflammatory cytokines may play a key role in the development of. Tumor Necrosis Factor-α Variations in Depression depression [3]. This theory well-explained some phenomena of psycho-neuroimmunological dysfunction in patients with MDD, who have an abnormal peripheral immune system [4]. It has been established that inflammatory cytokines can induce immune stimulation, which induces depression-like signs and symptoms, and these links have been supported by experimental and clinical evidences [5, 6]
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